UPDATED GUIDELINES FOR DIAGNOSIS AND MANAGEMENT OF ADULT DIABETIC KETOACIDOSIS

Abstract

Insulin and glucagon are potent regulators of glucose metabolism. For decades we have viewed diabetes from a bi-hormonal perspective of glucose regulation. This perspective is incomplete and inadequate in explaining some of the difficulties that patients and practitioners face when attempting to tightly control blood glucose concentrations. Intensively managing diabetes with insulin is fraught with frustration and risk. Despite our best efforts glucose fluctuations are unpredictable and hypoglycemia and weight gain are common. These challenges may be a result of deficiencies or abnormalities in other gluco-regulatory hormones. New understanding of the roles of other pancreatic and incretin hormones has led to a multi-hormonal view of glucose homeostasis. Diabetes is a general term for disorders characterised by polyuria. It usually refers to diabetes mellitus a common chronic syndrome of impaired carbohydrate, protein, and fat metabolism owing to insufficient secretion of insulin and/or target-tissue insulin resistance. Complications of diabetes mellitus include both macrovascular (cardiovascular) and microvascular (retinopathy, nephropathy or neuropathy) sequelae. Diabetic ketoacidosis (DKA) is characterised by a biochemical triad of hyperglycemia, ketonemia and acidemia with rapid symptom onset. An acute metabolic complication of diabetes that is potentially fatal if not properly treated. Common symptoms and signs include polyuria, polydipsia, polyphagia, weakness, weight loss, tachycardia, dry mucous membranes, poor skin turgor, hypotension, and in severe cases shock. Successful treatment includes correction of volume depletion, hyperglycemia, electrolyte imbalances and comorbid precipitating events with frequent monitoring and prevention. Complications of treatment include hypoglycemia, hypokalemia, hypoxemia and rarely pulmonary oedema. Cerebral oedema a rare but potentially rapidly fatal complication, occurs mainly in children. It is prevented by avoiding overly rapid fluid and electrolyte replacement.